What is the process for submitting a presubmission inquiry to PNAS?

What is the PNAS page estimator tool used for and how can it help in estimating the number of pages required for a manuscript submission to the Proceedings of the National Academy of Sciences (PNAS)?

The PNAS page estimator tool is used to estimate the number of pages needed for a manuscript submission to the Proceedings of the National Academy of Sciences (PNAS). It helps authors plan their submissions by providing an approximate page count based on the number of figures, tables, and references included in the manuscript. This tool can assist authors in preparing their manuscripts to meet the journal's formatting requirements and ensure that their work fits within the specified page limits.

How to cite PNAS in a research paper?

To cite a paper from the Proceedings of the National Academy of Sciences (PNAS) in a research paper, follow this format: Author(s). (Year). Title of the article. Proceedings of the National Academy of Sciences, Volume Number(Issue Number), Page Range. DOI.

What journal is PANS?

The journal PNAS is the journal of the Proceedings of the National Academy of Sciences. The first issue was published in 1915.

Is kerosene a hazardous waste material?

Kerosene is a light oil distilled from petroleum or shale oil and consists of a complex mixture of several hydrocarbons, no one of which stands out as a primary hazardous constituent. Constituents include, in alphabetical order:BenzeneButadieneCyclohexaneCyclohexeneCyclopropaneEthyl benzeneMethylcyclohexenen-Heptanen-HexaneNaphthalenePolynuclear aromatic hydrocarbons (PAHs, PNAs)TolueneXylenesAlthough benzene may be specifically removed before the product is marketed.

What is similar between an amoeba and volvox?

Both live in wet or moist environments, also, have membranes structures, nucleus, and other internal. P.S If your smart enough, you would put this answer and cheat. Trust me, it's right. I'm to smart to be wrong

How do forms of government and decision-making reflect a society’s worldview?

How do forms of government and decision-making reflect a society’s worldview? Forms of government and decision-making reflect a society’s worldview by determining the type of laws, policies, and procedures that the society accepts and follows. For example, a society that holds a collective worldview would likely have a form of government that emphasizes the collective good, such as socialism, whereas a society with an individualistic worldview would likely have a form of government that emphasizes individual rights, such as a democracy. Similarly, decisions made by a society’s government will reflect its worldview. A society with a collective worldview will likely make decisions that focus on the collective good, while a society with an individualistic worldview will likely make decisions that focus on individual rights and freedoms. References; pnas.org/doi/10.1073/pnas.1916936117 facinghistory.org/resource-library/individual-and-society

How do trichinella reproduce?

Sleeping sickness is also known as trypanosomiasis or African sleeping sickness. It's caused by a small parasite that leads to a serious infection in the brain and the meninges (the covering of the brain and spinal cord) and death if not treated. It is transmitted by the tsetse fly. They usually reproduce through binary fission (dividing into two). Now there is some evidence that they do reproduce sexually as well.Reference: L. Peacock, V. Ferris, R. Sharma, J. Sunter, M. Bailey, M. Carrington, W. Gibson. Identification of the meiotic life cycle stage of Trypanosoma brucei in the tsetse fly. Proceedings of the National Academy of Sciences, 2011; DOI: 10.1073/pnas.1019423108

Do oranges cure lung cancer?

No.Oranges contain vitamin C, which has been shown to have some potential anti-cancer benefits. However, these studies were done with intravenously injected vitamin C, as absorbing a clinically beneficial quantity from food such as oranges is impossible.Additionally, vitamin C has only been scientifically proven to work on mice and rats, and even then it only prolongs their life. It cannot cure them.So oranges are not going to cure cancer. I'm sorry.References:Mark Levine, Michael Graham Espey, Qi Chen (2009) Losing and finding a way at C: New promise for pharmacologic ascorbate in cancer treatment. Free Radical Biology & Medicine47: 27-29Qi Chen, Michael Graham Espey, Andrew Y. Sun, Chaya Pooput, Kenneth L. Kirk, Murali C. Krishna, Deena Beneda Khosh, Jeanne Drisko, and Mark Levine (2008) Pharmacologic doses of ascorbate act as a prooxidantand decrease growth of aggressive tumor xenograftsin mice. PNAS August 12, 2008 vol. 105 no. 32 11105-11109Wang-Jae Lee (2009) The Prospects of Vitamin C in Cancer Therapy. Immune Network 9:147-152

Is oranges good for lung cancer?

No.Oranges contain vitamin C, which has been shown to have some potential anti-cancer benefits. However, these studies were done with intravenously injected vitamin C, as absorbing a clinically beneficial quantity from food such as oranges is impossible.Additionally, vitamin C has only been scientifically proven to work on mice and rats, and even then it only prolongs their life. It cannot cure them.So oranges are not going to cure cancer. I'm sorry.References:Mark Levine, Michael Graham Espey, Qi Chen (2009) Losing and finding a way at C: New promise for pharmacologic ascorbate in cancer treatment. Free Radical Biology & Medicine47: 27-29Qi Chen, Michael Graham Espey, Andrew Y. Sun, Chaya Pooput, Kenneth L. Kirk, Murali C. Krishna, Deena Beneda Khosh, Jeanne Drisko, and Mark Levine (2008) Pharmacologic doses of ascorbate act as a prooxidantand decrease growth of aggressive tumor xenograftsin mice. PNAS August 12, 2008 vol. 105 no. 32 11105-11109Wang-Jae Lee (2009) The Prospects of Vitamin C in Cancer Therapy. Immune Network 9:147-152

What causes the roots to grow downward?

The roots of plants and trees grow into the ground for a number of reasons. Firstly it is to maintain stability so they don't collapse and secondly they grow to to find water and absorb the water that is in the ground.

What is the results of a mutation?

Mutations are changes in the DNA sequence of a cell's genome and are caused by radiation, viruses, transposons and mutagenic chemicals, as well as errors that occur during meiosis or DNA replication.[1][2][3] They can also be induced by the organism itself, by cellular processes such as hypermutation.Mutation can result in several different types of change in DNA sequences; these can either have no effect, alter the product of a gene, or prevent the gene from functioning. Studies in the fly Drosophila melanogaster suggest that if a mutation changes a protein produced by a gene, this will probably be harmful, with about 70 percent of these mutations having damaging effects, and the remainder being either neutral or weakly beneficial.[4] Due to the damaging effects that mutations can have on cells, organisms have evolved mechanisms such as DNA repair to remove mutations.[1] Therefore, the optimal mutation rate for a species is a trade-off between costs of a high mutation rate, such as deleterious mutations, and the metabolic costs of maintaining systems to reduce the mutation rate, such as DNA repair enzymes.[5] Viruses that use RNA as their genetic material have rapid mutation rates,[6] which can be an advantage since these viruses will evolve constantly and rapidly, and thus evade the defensive responses of e.g. the human immune system.[7]Mutations can involve large sections of DNA becoming duplicated, usually through genetic recombination.[8] These duplications are a major source of raw material for evolving new genes, with tens to hundreds of genes duplicated in animal genomes every million years.[9] Most genes belong to larger families of genes of shared ancestry.[10] Novel genes are produced by several methods, commonly through the duplication and mutation of an ancestral gene, or by recombining parts of different genes to form new combinations with new functions.[11][12] Here, domains act as modules, each with a particular and independent function, that can be mixed together to produce genes encoding new proteins with novel properties.[13] For example, the human eye uses four genes to make structures that sense light: three for color vision and one for night vision; all four arose from a single ancestral gene.[14] Another advantage of duplicating a gene (or even an entire genome) is that this increases redundancy; this allows one gene in the pair to acquire a new function while the other copy performs the original function.[15][16] Other types of mutation occasionally create new genes from previously noncoding DNA.[17][18]Changes in chromosome number may involve even larger mutations, where segments of the DNA within chromosomes break and then rearrange. For example, two chromosomes in the Homo genus fused to produce human chromosome 2; this fusion did not occur in the lineage of the other apes, and they retain these separate chromosomes.[19] In evolution, the most important role of such chromosomal rearrangements may be to accelerate the divergence of a population into new species by making populations less likely to interbreed, and thereby preserving genetic differences between these populations.[20]Sequences of DNA that can move about the genome, such as transposons, make up a major fraction of the genetic material of plants and animals, and may have been important in the evolution of genomes.[21] For example, more than a million copies of the Alu sequence are present in the human genome, and these sequences have now been recruited to perform functions such as regulating gene expression.[22] Another effect of these mobile DNA sequences is that when they move within a genome, they can mutate or delete existing genes and thereby produce genetic diversity.[2]In multicellular organisms with dedicated reproductive cells, mutations can be subdivided into germ line mutations, which can be passed on to descendants through their reproductive cells, and somatic mutations, which involve cells outside the dedicated reproductive group and which are not usually transmitted to descendants. If the organism can reproduce asexually through mechanisms such as cuttings or budding the distinction can become blurred.For example, plants can sometimes transmit somatic mutations to their descendants asexually or sexually where flower buds develop in somatically mutated parts of plants. A new mutation that was not inherited from either parent is called a de novo mutation. The source of the mutation is unrelated to the consequence[clarification needed], although the consequences are related to which cells were mutated.Nonlethal mutations accumulate within the gene pool and increase the amount of genetic variation[23]. The abundance of some genetic changes within the gene pool can be reduced by natural selection, while other "more favorable" mutations may accumulate and result in adaptive evolutionary changes.For example, a butterfly may produce offspring with new mutations. The majority of these mutations will have no effect; but one might change the color of one of the butterfly's offspring, making it harder (or easier) for predators to see. If this color change is advantageous, the chance of this butterfly surviving and producing its own offspring are a little better, and over time the number of butterflies with this mutation may form a larger percentage of the population.Neutral mutations are defined as mutations whose effects do not influence the fitness of an individual. These can accumulate over time due to genetic drift. It is believed that the overwhelming majority of mutations have no significant effect on an organism's fitness. Also, DNA repair mechanisms are able to mend most changes before they become permanent mutations, and many organisms have mechanisms for eliminating otherwise permanently mutated somatic cells.Mutation is generally accepted by biologists as the mechanism by which natural selection acts, generating advantageous new traits that survive and multiply in offspring as well as disadvantageous traits, in less fit offspring, that tend to die out.Contents[hide] 1 Classification of mutation types 1.1 By effect on structure1.2 By effect on function1.3 By effect on fitness1.4 By inheritance 1.4.1 By pattern of inheritance1.5 By impact on protein sequence1.6 Special classes1.7 Causes of mutation1.8 Nomenclature2 Harmful mutations3 Beneficial mutations4 Prion mutation5 See also6 References7 External linksClassification of mutation typesIllustrations of five types of chromosomal mutations. Selection of disease-causing mutations, in a standard table of the genetic code of amino acids.[24]By effect on structureThe sequence of a gene can be altered in a number of ways. Gene mutations have varying effects on health depending on where they occur and whether they alter the function of essential proteins. Mutations in the structure of genes can be classified as: Small-scale mutations, such as those affecting a small gene in one or a few nucleotides, including: Point mutations, often caused by chemicals or malfunction of DNA replication, exchange a single nucleotide for another[25]. These changes are classified as transitions or transversions[26]. Most common is the transition that exchanges a purine for a purine (A ↔ G) or a pyrimidine for a pyrimidine, (C ↔ T). A transition can be caused by nitrous acid, base mis-pairing, or mutagenic base analogs such as 5-bromo-2-deoxyuridine (BrdU). Less common is a transversion, which exchanges a purine for a pyrimidine or a pyrimidine for a purine (C/T ↔ A/G). An example of a transversion is adenine (A) being converted into a cytosine (C). A point mutation can be reversed by another point mutation, in which the nucleotide is changed back to its original state (true reversion) or by second-site reversion (a complementary mutation elsewhere that results in regained gene functionality). Point mutations that occur within the protein coding region of a gene may be classified into three kinds, depending upon what the erroneous codon codes for: Silent mutations: which code for the same amino acid.Missense mutations: which code for a different amino acid.Nonsense mutations: which code for a stop and can truncate the protein.Insertions add one or more extra nucleotides into the DNA. They are usually caused by transposable elements, or errors during replication of repeating elements (e.g. AT repeats[citation needed]). Insertions in the coding region of a gene may alter splicing of the mRNA (splice site mutation), or cause a shift in the reading frame (frameshift), both of which can significantly alter the gene product. Insertions can be reverted by excision of the transposable element.Deletions remove one or more nucleotides from the DNA. Like insertions, these mutations can alter the reading frame of the gene. They are generally irreversible: though exactly the same sequence might theoretically be restored by an insertion, transposable elements able to revert a very short deletion (say 1-2 bases) in any location are either highly unlikely to exist or do not exist at all. Note that a deletion is not the exact opposite of an insertion: the former is quite random while the latter consists of a specific sequence inserting at locations that are not entirely random or even quite narrowly defined.Large-scale mutations in chromosomal structure, including: Amplifications (or gene duplications) leading to multiple copies of all chromosomal regions, increasing the dosage of the genes located within them.Deletions of large chromosomal regions, leading to loss of the genes within those regions.Mutations whose effect is to juxtapose previously separate pieces of DNA, potentially bringing together separate genes to form functionally distinct fusion genes (e.g. bcr-abl). These include: Chromosomal translocations: interchange of genetic parts from nonhomologous chromosomes.Interstitial deletions: an intra-chromosomal deletion that removes a segment of DNA from a single chromosome, thereby apposing previously distant genes. For example, cells isolated from a human astrocytoma, a type of brain tumor, were found to have a chromosomal deletion removing sequences between the "fused in glioblastoma" (fig) gene and the receptor tyrosine kinase "ros", producing a fusion protein (FIG-ROS). The abnormal FIG-ROS fusion protein has constitutively active kinase activity that causes oncogenic transformation (a transformation from normal cells to cancer cells).Chromosomal inversions: reversing the orientation of a chromosomal segment.Loss of heterozygosity: loss of one allele, either by a deletion or recombination event, in an organism that previously had two different alleles.By effect on functionLoss-of-function mutations are the result of gene product having less or no function. When the allele has a complete loss of function (null allele) it is often called an amorphic mutation. Phenotypes associated with such mutations are most often recessive. Exceptions are when the organism is haploid, or when the reduced dosage of a normal gene product is not enough for a normal phenotype (this is called haploinsufficiency).Gain-of-function mutations change the gene product such that it gains a new and abnormal function. These mutations usually have dominant phenotypes. Often called a neomorphic mutation.Dominant negative mutations (also called antimorphic mutations) have an altered gene product that acts antagonistically to the wild-type allele. These mutations usually result in an altered molecular function (often inactive) and are characterised by a dominant or semi-dominant phenotype. In humans, Marfan syndrome is an example of a dominant negative mutation occurring in an autosomal dominant disease. In this condition, the defective glycoprotein product of the fibrillin gene (FBN1) antagonizes the product of the normal allele.Lethal mutations are mutations that lead to the death of the organisms which carry the mutations.A back mutation or reversion is a point mutation that restores the original sequence and hence the original phenotype.[27]By effect on fitnessIn applied genetics it is usual to speak of mutations as either harmful or beneficial. A harmful mutation is a mutation that decreases the fitness of the organism.A beneficial mutation is a mutation that increases fitness of the organism, or which promotes traits that are desirable.In theoretical population genetics, it is more usual to speak of such mutations as deleterious or advantageous. In the neutral theory of molecular evolution, genetic drift is the basis for most variation at the molecular level.A neutral mutation has no harmful or beneficial effect on the organism. Such mutations occur at a steady rate, forming the basis for the molecular clock.A deleterious mutation has a negative effect on the phenotype, and thus decreases the fitness of the organism.An advantageous mutation has a positive effect on the phenotype, and thus increases the fitness of the organism.A nearly neutral mutation is a mutation that may be slightly deleterious or advantageous, although most nearly neutral mutations are slightly deleterious.By inheritanceinheritable generic in pro-generic tissue or cells on path to be changed to gametes.non inheritable somatic (eg, carcinogenic mutation)non inheritable post mortem aDNA mutation in decaying remains.By pattern of inheritanceThe human genome contains two copies of each gene - a paternal and a maternal allele. A heterozygous mutation is a mutation of only one allele.A homozygous mutation is an identical mutation of both the paternal and maternal alleles.Compound heterozygous mutations or a genetic compound comprises two different mutations in the paternal and maternal alleles.[28]A wildtype or homozygous non-mutated organism is one in which neither allele is mutated. (Just not a mutation)By impact on protein sequenceA frameshift mutation is a mutation caused by insertion or deletion of a number of nucleotides that is not evenly divisible by three from a DNA sequence. Due to the triplet nature of gene expression by codons, the insertion or deletion can disrupt the reading frame, or the grouping of the codons, resulting in a completely different translation from the original. The earlier in the sequence the deletion or insertion occurs, the more altered the protein produced is.A nonsense mutation is a point mutation in a sequence of DNA that results in a premature stop codon, or a nonsense codon in the transcribed mRNA, and possibly a truncated, and often nonfunctional protein product.Missense mutations or nonsynonymous mutations are types of point mutations where a single nucleotide is changed to cause substitution of a different amino acid. This in turn can render the resulting protein nonfunctional. Such mutations are responsible for diseases such as Epidermolysis bullosa, sickle-cell disease, and SOD1 mediated ALS (Boillée 2006, p. 39).A neutral mutation is a mutation that occurs in an amino acid codon which results in the use of a different, but chemically similar, amino acid. The similarity between the two is enough that little or no change is often rendered in the protein. For example, a change from AAA to AGA will encode lysine, a chemically similar molecule to the intended arginine.Silent mutations are mutations that do not result in a change to the amino acid sequence of a protein. They may occur in a region that does not code for a protein, or they may occur within a codon in a manner that does not alter the final amino acid sequence. The phrase silent mutation is often used interchangeably with the phrase synonymous mutation; however, synonymous mutations are a subcategory of the former, occurring only within exons. The name silent could be a misnomer. For example, a silent mutation in the exon/intron border may lead to alternative splicing by changing the splice site (see Splice site mutation), thereby leading to a changed protein.Special classesConditional mutation is a mutation that has wild-type (or less severe) phenotype under certain "permissive" environmental conditions and a mutant phenotype under certain "restrictive" conditions. For example, a temperature-sensitive mutation can cause cell death at high temperature (restrictive condition), but might have no deleterious consequences at a lower temperature (permissive condition).Causes of mutationTwo classes of mutations are spontaneous mutations (molecular decay) and induced mutations caused by mutagens. Spontaneous mutations on the molecular level include:Tautomerism - A base is changed by the repositioning of a hydrogen atom, altering the hydrogen bonding pattern of that base resulting in incorrect base pairing during replication.Depurination - Loss of a purine base (A or G) to form an apurinic site (AP site).Deamination - Hydrolysis changes a normal base to an atypical base containing a keto group in place of the original amine group. Examples include C → U and A → HX (hypoxanthine), which can be corrected by DNA repair mechanisms; and 5MeC (5-methylcytosine) → T, which is less likely to be detected as a mutation because thymine is a normal DNA base.Transition - A purine changes to another purine, or a pyrimidine to a pyrimidine.Transversion - A purine becomes a pyrimidine, or vice versa.A covalent adduct between benzo[a]pyrene, the major mutagen in tobacco smoke, and DNA[29] Induced mutations on the molecular level can be caused by:Chemicals Hydroxylamine NH2OHBase analogs (e.g. BrdU)Alkylating agents (e.g. N-ethyl-N-nitrosourea) These agents can mutate both replicating and non-replicating DNA. In contrast, a base analog can only mutate the DNA when the analog is incorporated in replicating the DNA. Each of these classes of chemical mutagens has certain effects that then lead to transitions, transversions, or deletions.Agents that form DNA adducts (e.g. ochratoxin A metabolites)[30]DNA intercalating agents (e.g. ethidium bromide)DNA crosslinkersOxidative damageNitrous acid converts amine groups on A and C to diazo groups, altering their hydrogen bonding patterns which leads to incorrect base pairing during replication.Radiation Ultraviolet radiation (nonionizing radiation). Two nucleotide bases in DNA - cytosine and thymine - are most vulnerable to radiation that can change their properties. UV light can induce adjacent thymine bases in a DNA strand to pair with each other, as a bulky dimer.Ionizing radiationViral infections[31]DNA has so-called hotspots, where mutations occur up to 100 times more frequently than the normal mutation rate. A hotspot can be at an unusual base, e.g., 5-methylcytosine.Mutation rates also vary across species. Evolutionary biologists have theorized that higher mutation rates are beneficial in some situations, because they allow organisms to evolve and therefore adapt more quickly to their environments. For example, repeated exposure of bacteria to antibiotics, and selection of resistant mutants, can result in the selection of bacteria that have a much higher mutation rate than the original population (mutator strains).NomenclatureNomenclature of mutations specify the type of mutation and base or amino acid changes. Nucleotide substitution (e.g. 76A>T) - The number is the position of the nucleotide from the 5' end, the first letter represents the wild type nucleotide, and the second letter represents the nucleotide which replaced the wild type. In the given example, the adenine at the 76th position was replaced by a thymine. If it becomes necessary to differentiate between mutations in genomic DNA, mitochondrial DNA, and RNA, a simple convention is used. For example, if the 100th base of a nucleotide sequence mutated from G to C, then it would be written as g.100G>C if the mutation occurred in genomic DNA, m.100G>C if the mutation occurred in mitochondrial DNA, or r.100g>c if the mutation occurred in RNA. Note that for mutations in RNA, the nucleotide code is written in lower case.Amino acid substitution (e.g. D111E) - The first letter is the one letter code of the wild type amino acid, the number is the position of the amino acid from the N terminus, and the second letter is the one letter code of the amino acid present in the mutation. Nonsense mutations are represented with an X for the second amino acid (e.g. D111X).Amino acid deletion (e.g. ΔF508) - The Greek letter Δ (delta) indicates a deletion. The letter refers to the amino acid present in the wild type and the number is the position from the N terminus of the amino acid were it to be present as in the wild type.Harmful mutationsChanges in DNA caused by mutation can cause errors in protein sequence, creating partially or completely non-functional proteins. To function correctly, each cell depends on thousands of proteins to function in the right places at the right times. When a mutation alters a protein that plays a critical role in the body, a medical condition can result. A condition caused by mutations in one or more genes is called a genetic disorder. Some mutations alter a gene's DNA base sequence but do not change the function of the protein made by the gene. Studies of the fly Drosophila melanogaster suggest that if a mutation does change a protein, this will probably be harmful, with about 70 percent of these mutations having damaging effects, and the remainder being either neutral or weakly beneficial.[32] However, studies in yeast have shown that only 7% of mutations that are not in genes are harmful.[33] If a mutation is present in a germ cell, it can give rise to offspring that carries the mutation in all of its cells. This is the case in hereditary diseases. On the other hand, a mutation may occur in a somatic cell of an organism. Such mutations will be present in all descendants of this cell within the same organism, and certain mutations can cause the cell to become malignant, and thus cause cancer[34].Often, gene mutations that could cause a genetic disorder are repaired by the DNA repair system of the cell. Each cell has a number of pathways through which enzymes recognize and repair mistakes in DNA. Because DNA can be damaged or mutated in many ways, the process of DNA repair is an important way in which the body protects itself from disease.Beneficial mutationsAlthough most mutations that change protein sequences are harmful, some mutations have a positive effect on an organism. In this case, the mutation may enable the mutant organism to withstand particular environmental stresses better than wild-type organisms, or reproduce more quickly. In these cases a mutation will tend to become more common in a population through natural selection. For example, a specific 32 base pair deletion in human CCR5 (CCR5-Δ32) confers HIV resistance to homozygotes and delays AIDS onset in heterozygotes.[35] The CCR5 mutation is more common in those of European descent. One possible explanation of the etiology of the relatively high frequency of CCR5-Δ32 in the European population is that it conferred resistance to the bubonic plague in mid-14th century Europe. People with this mutation were more likely to survive infection; thus its frequency in the population increased.[36] This theory could explain why this mutation is not found in Africa, where the bubonic plague never reached. A newer theory suggests that the selective pressure on the CCR5 Delta 32 mutation was caused by smallpox instead of the bubonic plague.[37]Prion mutationPrions are proteins and don't contain genetic material, however prion replication has been shown to be subject to mutationand natural selection just like other forms of replication.[38] See alsoAneuploidyAntioxidantBudgerigar colour geneticsHomeoboxMacromutationMuller's morphsMutantPolyploidyRobertsonian translocationSignature tagged mutagenesisSite-directed mutagenesisTILLING (molecular biology)References^ a b Bertram J (2000). "The molecular biology of cancer". Mol. Aspects Med. 21(6): 167-223. doi:10.1016/S0098-2997(00)00007-8. PMID 11173079.^ a b Aminetzach YT, Macpherson JM, Petrov DA (2005). "Pesticide resistance via transposition-mediated adaptive gene truncation in Drosophila". Science 309(5735): 764-7. doi:10.1126/science.1112699. PMID 16051794.^ Burrus V, Waldor M (2004). "Shaping bacterial genomes with integrative and conjugative elements". Res. Microbiol.155 (5): 376-86. doi:10.1016/j.resmic.2004.01.012. PMID 15207870.^ Sawyer SA, Parsch J, Zhang Z, Hartl DL (2007). "Prevalence of positive selection among nearly neutral amino acid replacements in Drosophila". Proc. Natl. Acad. Sci. U.S.A.104 (16): 6504-10. doi:10.1073/pnas.0701572104. PMID 17409186.^ Sniegowski P, Gerrish P, Johnson T, Shaver A (2000). "The evolution of mutation rates: separating causes from consequences". Bioessays 22 (12): 1057-66. doi:10.1002/1521-1878(200012)22:123.0.CO;2-W. PMID 11084621.^ Drake JW, Holland JJ (1999). "Mutation rates among RNA viruses". Proc. Natl. Acad. Sci. U.S.A. 96 (24): 13910-3. doi:10.1073/pnas.96.24.13910. PMID 10570172. PMC 24164. http://www.pnas.org/content/96/24/13910.long.^ Holland J, Spindler K, Horodyski F, Grabau E, Nichol S, VandePol S (1982). "Rapid evolution of RNA genomes". Science 215 (4540): 1577-85. doi:10.1126/science.7041255. PMID 7041255.^ Hastings, P J; Lupski, JR; Rosenberg, SM; Ira, G (2009). "Mechanisms of change in gene copy number". Nature Reviews. Genetics 10 (8): 551-564. doi:10.1038/nrg2593. PMID 19597530.^ Carroll SB, Grenier J, Weatherbee SD (2005). From DNA to Diversity: Molecular Genetics and the Evolution of Animal Design. Second Edition. Oxford: Blackwell Publishing. ISBN 1-4051-1950-0.^ Harrison P, Gerstein M (2002). "Studying genomes through the aeons: protein families, pseudogenes and proteome evolution". J Mol Biol 318 (5): 1155-74. doi:10.1016/S0022-2836(02)00109-2. PMID 12083509.^ Orengo CA, Thornton JM (2005). "Protein families and their evolution-a structural perspective". Annu. Rev. Biochem. 74: 867-900. doi:10.1146/annurev.biochem.74.082803.133029. PMID 15954844.^ Long M, Betrán E, Thornton K, Wang W (November 2003). "The origin of new genes: glimpses from the young and old". Nat. Rev. Genet. 4 (11): 865-75. doi:10.1038/nrg1204. PMID 14634634.^ Wang M, Caetano-Anollés G (2009). "The evolutionary mechanics of domain organization in proteomes and the rise of modularity in the protein world". Structure 17 (1): 66-78. doi:10.1016/j.str.2008.11.008. PMID 19141283.^ Bowmaker JK (1998). "Evolution of colour vision in vertebrates". Eye (London, England) 12 (Pt 3b): 541-7. PMID 9775215.^ Gregory TR, Hebert PD (1999). "The modulation of DNA content: proximate causes and ultimate consequences". Genome Res. 9 (4): 317-24. doi:10.1101/gr.9.4.317 (inactive 2009-11-14). PMID 10207154. http://genome.cshlp.org/content/9/4/317.full.^ Hurles M (July 2004). "Gene duplication: the genomic trade in spare parts". PLoS Biol. 2 (7): E206. doi:10.1371/journal.pbio.0020206. PMID 15252449.^ Liu N, Okamura K, Tyler DM (2008). "The evolution and functional diversification of animal microRNA genes". Cell Res. 18 (10): 985-96. doi:10.1038/cr.2008.278. PMID 18711447. PMC 2712117. http://www.nature.com/cr/journal/v18/n10/full/cr2008278a.html.^ Siepel A (October 2009). "Darwinian alchemy: Human genes from noncoding DNA". Genome Res. 19 (10): 1693-5. doi:10.1101/gr.098376.109. PMID 19797681. PMC 2765273. http://genome.cshlp.org/content/19/10/1693.full.^ Zhang J, Wang X, Podlaha O (2004). "Testing the chromosomal speciation hypothesis for humans and chimpanzees". Genome Res. 14 (5): 845-51. doi:10.1101/gr.1891104. PMID 15123584.^ Ayala FJ, Coluzzi M (2005). "Chromosome speciation: humans, Drosophila, and mosquitoes". Proc. Natl. Acad. Sci. U.S.A. 102 (Suppl 1): 6535-42. doi:10.1073/pnas.0501847102. PMID 15851677. PMC 1131864. http://www.pnas.org/content/102/suppl.1/6535.full.^ Hurst GD, Werren JH (2001). "The role of selfish genetic elements in eukaryotic evolution". Nat. Rev. Genet.2 (8): 597-606. doi:10.1038/35084545. PMID 11483984.^ Häsler J, Strub K (2006). "Alu elements as regulators of gene expression". Nucleic Acids Res. 34 (19): 5491-7. doi:10.1093/nar/gkl706. PMID 17020921.^ Eyre-Walker, A.; Keightley, P. (Aug 2007). "The distribution of fitness effects of new mutations". Nature reviews. Genetics 8 (8): 610-618. doi:10.1038/nrg2146. ISSN 1471-0056. PMID 17637733. edit^ References for the image are found in Wikimedia Commons page at: Commons:File:Notable mutations.svg#References.^ Freese, Ernst (April 1959). "The Difference between Spontaneous and Base-Analogue Induced Mutations of Phage T4". Proc. Natl. Acad. Sci. U.S.A. 45 (4): 622-33. doi:10.1073/pnas.45.4.622. PMID 16590424.^ Freese, Ernst (1959). "The Specific Mutagenic Effect of Base Analogues on Phage T4". J. Mol. Biol. 1: 87-105. doi:10.1016/S0022-2836(59)80038-3.^ Ellis NA, Ciocci S, German J (2001). "Back mutation can produce phenotype reversion in Bloom syndrome somatic cells". Hum Genet 108 (2): 167-73. doi:10.1007/s004390000447. PMID 11281456. http://link.springer.de/link/service/journals/00439/bibs/1108002/11080167.htm.^ Medterms.com^ Created from PDB 1JDG^ Pfohl-Leszkowicz A, Manderville RA (January 2007). "Ochratoxin A: An overview on toxicity and carcinogenicity in animals and humans". Mol Nutr Food Res 51 (1): 61-99. doi:10.1002/mnfr.200600137. PMID 17195275.^ Pilon L, Langelier Y, Royal A (1 August 1986). "Herpes simplex virus type 2 mutagenesis: characterization of mutants induced at the hprt locus of nonpermissive XC cells". Mol. Cell. Biol. 6 (8): 2977-83. PMID 3023954. PMC 367868. http://mcb.asm.org/cgi/pmidlookup?view=long&pmid=3023954.^ Sawyer SA, Parsch J, Zhang Z, Hartl DL (2007). "Prevalence of positive selection among nearly neutral amino acid replacements in Drosophila". Proc. Natl. Acad. Sci. U.S.A.104 (16): 6504-10. doi:10.1073/pnas.0701572104. PMID 17409186.^ Doniger SW, Kim HS, Swain D, et al. (August 2008). "A catalog of neutral and deleterious polymorphism in yeast". PLoS Genet. 4 (8): e1000183. doi:10.1371/journal.pgen.1000183. PMID 18769710.^ Ionov Y, Peinado MA, Malkhosyan S, Shibata D, Perucho M (1993). "Ubiquitous somatic mutations in simple repeated sequences reveal a new mechanism for colonic carcinogenesis". Nature 363 (6429): 558-61. doi:10.1038/363558a0. PMID 8505985.^ "CCR5 receptor gene and HIV infection, Antonio Pacheco.". http://www.cdc.gov/genomics/hugenet/factsheets/FS_CCR5.htm.^ "PBS:Secrets of the Dead. Case File: Mystery of the Black Death". http://www.pbs.org/wnet/secrets/previous_seasons/case_plague/clues.html.^ Galvani A, Slatkin M (2003). "Evaluating plague and smallpox as historical selective pressures for the CCR5-Δ32 HIV-resistance allele". Proc Natl Acad Sci USA 100(25): 15276-9. doi:10.1073/pnas.2435085100. PMID 14645720.^ 'Lifeless' prion proteins are 'capable of evolution'External links"All About Mutations" from the Huntington's Disease Outreach Project for Education at StanfordCentral Locus Specific Variation Database at the Institute of Genomics and Integrative BiologyThe mutations chapter of the WikiBooks General Biology textbookExamples of Beneficial MutationsCorrecting mutation by gene therapyBBC Radio 4 In Our Time - GENETIC MUTATION - with Steve Jones - streaming audio

How do you get people to stop sleeping in your bed when your away?

Symbiosis From Wikipedia, the free encyclopedia"Symbiology" redirects here. For use of things that represent other things by association, resemblance, or convention, see Symbology.This article is about the biological phenomenon. For other uses, see Symbiosis (disambiguation). For the Marvel character, see Symbiote (comics).In a symbiotic mutualism, the clownfishfeeds on small invertebrates that otherwise have potential to harm the sea anemone, and the fecal matter from the clownfish provides nutrients to the sea anemone. The clownfish is additionally protected from predators by the anemone's stinging cells, to which the clownfish is immune.Symbiosis (from Ancient Greek σύν "together" and βίωσι&sigmaf; "living")[1]is close and often long-term interaction between different biological species. In 1877, Bennett used the word symbiosis (which previously had been used of people living together in community) to describe the mutualistic relationship in lichens.[2]In 1879, by the GermanmycologistHeinrich Anton de Bary, defined it as "the living together of unlike organisms."[3][4]The definition of symbiosis is controversial among scientists. Some believe symbiosis should only refer to persistent mutualisms, while others believe it should apply to any types of persistent biological interactions (i.e. mutualistic, commensalistic, or parasitic).[5]Some symbiotic relationships are obligate, meaning that both symbionts entirely depend on each other for survival. For example, many lichensconsist of fungal and photosynthetic symbionts that cannot live on their own.[3][6][7][8]Others are facultative, meaning that they can, but do not have to live with the other organism.Symbiotic relationships include those associations in which one organism lives on another (ectosymbiosis, such as mistletoe), or where one partner lives inside the other (endosymbiosis, such as lactobacilliand other bacteria in humans or zooxanthellesin corals).[9][10]Contents[hide] 1 Physical interaction2 Mutualism2.1 Mutualism and endosymbiosis3 Commensalism4 Parasitism5 Amensalism6 Symbiosis and evolution6.1 Vascular plants6.2 Symbiogenesis6.3 Co-evolution7 Notes8 See also9 References10 External links[edit]Physical interactionAlder tree root noduleEndosymbiosisis any symbiotic relationship in which one symbiont lives within the tissues of the other, either in the intracellular space or extracellularly.[10][11]Examples include diverse microbiomes, rhizobia, nitrogen-fixing bacteria that live in root noduleson legumeroots; actinomycetenitrogen-fixing bacteria called Frankia, which live in alder tree root nodules; single-celled algae inside reef-building corals; and bacterial endosymbionts that provide essential nutrients to about 10%-15% of insects.Ectosymbiosis, also referred to as exosymbiosis, is any symbiotic relationship in which the symbiont lives on the body surface of the host, including the inner surface of the digestivetract or the ducts of exocrineglands.[10][12]Examples of this include ectoparasitessuch as lice, commensalectosymbionts such as the barnaclesthat attach themselves to the jaw of baleen whales, and mutualistectosymbionts such as cleaner fish.[edit]MutualismMain article: Mutualism (biology)Hermit crab, Calcinus laevimanus, with sea anemone.Mutualism is any relationship between individuals of different species where both individuals derive a benefit.[13]In general, only lifelong interactions involving close physical and biochemicalcontact can properly be considered symbiotic. Mutualistic relationships may be either obligate for both species, obligate for one but facultative for the other, or facultative for both. Many biologistsrestrict the definition of symbiosis to close mutualist relationships.A large percentage of herbivoreshave mutualistic gut faunathat help them digest plant matter, which is more difficult to digest than animal prey.[9]Coral reefs are the result of mutualisms between coral organisms and various types of algae that live inside them.[14]Most land plants and land ecosystems rely on mutualisms between the plants, which fix carbon from the air, and mycorrhyzalfungi, which help in extracting minerals from the ground.[15]An example of mutual symbiosis is the relationship between the ocellaris clownfish that dwell among the tentacles of Ritteri sea anemones. The territorial fish protects the anemone from anemone-eating fish, and in turn the stingingtentacles of the anemone protect the clownfish from its predators. A special mucuson the clownfish protects it from the stinging tentacles.[16]Another example is the goby fish, which sometimes lives together with a shrimp. The shrimp digs and cleans up a burrow in the sand in which both the shrimp and the goby fish live. The shrimp is almost blind, leaving it vulnerable to predators when above ground. In case of danger the goby fish touches the shrimp with its tail to warn it. When that happens both the shrimp and goby fish quickly retreat into the burrow.[17]One of the most spectacular examples of obligate mutualism is between the siboglinidtube wormsand symbiotic bacteria that live at hydrothermal vents and cold seeps. The worm has no digestive tract and is wholly reliant on its internal symbionts for nutrition. The bacteria oxidize either hydrogen sulfide or methane, which the host supplies to them. These worms were discovered in the late 1980s at the hydrothermal vents near the Galapagos Islands and have since been found at deep-seahydrothermal vents and cold seeps in all of the world's oceans.[18]There are also many types of tropical and sub-tropical ants that have evolved very complex relationships with certain tree species.[19][edit]Mutualism and endosymbiosisDuring mutualistic symbioses, the host cell lacks some of the nutrients, which are provided by the endosymbiont. As a result, the host favors endosymbiont's growth processes within itself by producing some specialized cells. These cells affect the genetic composition of the host in order to regulate the increasing population of the endosymbionts and ensuring that these genetic changes are passed onto the offspring via vertical transmission (heredity).[20]Adaptation of the endosymbiont to the host's lifestyle leads to many changes in the endosymbiont - the foremost being drastic reduction in its genome size. This is due to many genes being lost during the process of metabolism, and DNA repair and recombination. While important genes participating in the DNA to RNA transcription, proteintranslationand DNA/RNA replication are retained. That is, a decrease in genome size is due to loss of protein coding genes and not due to lessening of inter-genic regions or open reading frame (ORF) size. Thus, species that are naturally evolving and contain reduced sizes of genes can be accounted for an increased number of noticeable differences between them, thereby leading to changes in their evolutionary rates. As the endosymbiotic bacteria related with these insects are passed on to the offspring strictly via vertical genetic transmission, intracellular bacteria goes through many hurdles during the process, resulting in the decrease in effective population sizes when compared to the free living bacteria. This incapability of the endosymbiotic bacteria to reinstate its wild type phenotype via a recombination process is called as Muller's ratchet phenomenon. Muller's ratchet phenomenon together with less effective population sizes has led to an accretion of deleterious mutations in the non-essential genes of the intracellular bacteria.[21]This could have been due to lack of selectionmechanisms prevailing in the rich environment of the host.[22][23][edit]CommensalismPhoreticmites on a fly (Pseudolynchia canariensis).Main article: CommensalismCommensalism describes a relationship between two living organisms where one benefits and the other is not significantly harmed or helped. It is derived from the English word commensalused of human social interaction. The word derives from the medieval Latin word, formed from com- and mensa, meaning "sharing a table".[13][24]Commensal relationships may involve one organism using another for transportation (phoresy) or for housing (inquilinism), or it may also involve one organism using something another created, after its death (metabiosis). Examples of metabiosis are hermit crabs using gastropodshells to protect their bodies and spiders building their webs on plants.[edit]ParasitismFlea bites on a human is an example of parasitism.Main article: ParasitismA parasiticrelationship is one in which one member of the association benefits while the other is harmed.[25]Parasitic symbioses take many forms, from endoparasitesthat live within the host's body to ectoparasitesthat live on its surface. In addition, parasites may be necrotrophic, which is to say they kill their host, or biotrophic, meaning they rely on their host's surviving. Biotrophic parasitism is an extremely successful mode of life. Depending on the definition used, as many as half of all animals have at least one parasitic phase in their life cycles, and it is also frequent in plants and fungi. Moreover, almost all free-living animals are host to one or more parasite taxa. An example of a biotrophic relationship would be a tick feeding on the blood of its host.[edit]AmensalismAmensalism is the type of relationship that exists where one species is inhibited or completely obliterated and one is unaffected. This type of symbiosis is relatively uncommon in rudimentary reference texts, but is omnipresent in the natural world. An example is a sapling growing under the shadow of a mature tree. The mature tree can begin to rob the sapling of necessary sunlight and, if the mature tree is very large, it can take up rainwater and deplete soil nutrients. Throughout the process the mature tree is unaffected. Indeed, if the sapling dies, the mature tree gains nutrients from the decaying sapling. Note that these nutrients become available because of the sapling's decomposition, rather than from the living sapling, which would be a case of parasitism.[edit]Symbiosis and evolutionLeafhoppersprotected by an army of meat antsWhile historically, symbiosis has received less attention than other interactions such as predation or competition,[26]it is increasingly recognized as an important selective force behind evolution,[9][27]with many species having a long history of interdependent co-evolution.[28]In fact, the evolution of alleukaryotes(plants, animals, fungi, and protists) is believed under the endosymbiotic theory to have resulted from a symbiosis between various sorts of bacteria.[9][29][30][edit]Vascular plantsAbout 80% of vascular plants worldwide form symbiotic relationships with fungi, for example, in arbuscular mycorrhizas.[31][edit]SymbiogenesisThe biologist Lynn Margulis, famous for her work on endosymbiosis, contends that symbiosis is a major driving force behind evolution. She considers Darwin'snotion of evolution, driven by competition, to be incomplete and claims that evolution is strongly based on co-operation, interaction, and mutual dependenceamong organisms. According to Margulis and Dorion Sagan, "Life did not take over the globe by combat, but by networking."[32][edit]Co-evolutionSymbiosis played a major role in the co-evolutionof floweringplants and the animals that pollinatethem. Many plants that are pollinated by insects, bats, orbirds have highly specialized flowers modified to promote pollination by a specific pollinator that is also correspondingly adapted. The first flowering plants in the fossil record had relatively simple flowers. Adaptive speciationquickly gave rise to many diverse groups of plants, and, at the same time, corresponding speciation occurred in certain insect groups. Some groups of plants developed nectar and large sticky pollen, while insects evolved more specialized morphologies to access and collect these rich food sources. In some taxa of plants and insects the relationship has become dependent,[33]where the plant species can only be pollinated by one species of insect.[34][edit]Notes^ σύν, βίωσι&sigmaf;. Liddell, Henry George; Scott, Robert; A Greek-English Lexicon at Perseus Project^"symbiosis". Oxford English Dictionary. Oxford University Press. 3rd ed. 2001.^ abWilkinson 2001^Douglas 1994, p. 1^Douglas, Angela E. (2010), The symbiotic habit, New Jersey: Princeton University Press, pp. 5-12, ISBN 978-0-691-11341-8^Isaac 1992, p. 266^Saffo 1993^Douglas, Angela E. (2010), The symbiotic habit, New Jersey: Princeton University Press, p. 4, ISBN 978-0-691-11341-8^ abcdMoran 2006^ abcAhmadjian & Paracer 2000, p. 12^Sapp 1994, p. 142^Nardon & Charles 2002^ abAhmadjian & Paracer 2000, p. 6^Toller, Rowan & Knowlton 2001^Harrison 2005^Lee 2003^Facey, Helfman & Collette 1997^Cordes 2005^Piper, Ross(2007), Extraordinary Animals: An Encyclopedia of Curious and Unusual Animals, Greenwood Press.^Latorre, A.; Durban, A., Moya, A. & Pereto, J. (2011). The role of symbiosis in eukaryotic evolution. Origins and evolution of life - An astrobiological perspective. pp. 326-339.^ Moran, N. A. (1996). "Accelerated evolution and Muller's ratchet in endosymbiotic bacteria.". Proceedings of the National Academy of Sciences of the United States of America 93: 2873-2878. DOI:10.1073/pnas.93.7.2873.PMC 39726. PMID 8610134.^Andersson, S.G.; Kurland, C.G. (1998). "Reductive evolution of resident genomes.". Trends in Microbiology 6: 263-268.^Wernegreen, J.J. (2002). "Genome evolution in bacterial endosymbionts of insects.". Nature reviews, Genetics3: 850-861.^Nair 2005^Ahmadjian & Paracer 2000, p. 7^Townsend, Begon & Harper 1996^Wernegreen 2004^Ahmadjian & Paracer 2000, pp. 3-4^Brinkman 2002^Golding & Gupta 1995^Schüßler, A. et al. (2001), "A new fungal phylum, theGlomeromycota: phylogeny and evolution", Mycol. Res.105 (12): 1416, DOI:10.1017/S0953756201005196.^Sagan & Margulis 1986^Harrison 2002^Danforth & Ascher 1997[edit]See alsoAnagenesisAposymbioticAquaponicsCheating (biology)Cleaning symbiosisDecompicultureHuman Microbiome ProjectList of symbiotic organismsList of symbiotic relationshipsMicrobiomeMultigenomic organismSymbiogenesisSymbiosis (chemical)[edit]ReferencesAhmadjian, Vernon; Paracer, Surindar (2000), Symbiosis: an introduction to biological associations, Oxford [Oxfordshire]: Oxford University Press, ISBN 0-19-511806-5Burgess, Jeremy (1994), Forum: What's in it for me, New ScientistBoucher, Douglas H (1988), The Biology of Mutualism: Ecology and Evolution, New York: Oxford University Press, ISBN 0-19-505392-3Cordes, E.E.; Arthur, M.A.; Shea, K.; Arvidson, R.S.; Fisher, C.R. (2005), "Modeling the mutualistic interactions between tubeworms and microbial consortia", PLoS Biol 3 (3): 1-10,DOI:10.1371/journal.pbio.0030077, PMC 1044833,PMID 15736979Brinkman, F.S.L.; Blanchard, J.L.; Cherkasov, A.; Av-gay, Y.; Brunham, R.C.; Fernandez, R.C.; Finlay, B.B.; Otto, S.P.; Ouellette, B.F.F.; Keeling, P.J.; Others, (2002), "Evidence That Plant-Like Genes in Chlamydia Species Reflect an Ancestral Relationship between Chlamydiaceae, Cyanobacteria, and the Chloroplast", Genome Research 12 (8): 1159-1167,DOI:10.1101/gr.341802, PMC 186644, PMID 12176923, retrieved 2007-09-30Danforth, B.N.; Ascher, J. (1997), "Flowers and Insect Evolution", Science 283(5399): 143,DOI:10.1126/science.283.5399.143a, retrieved 2007-09-25Douglas, Angela (2010), The Symbiotic Habit, Princeton University Press, ISBN 0-19-854294-1Douglas, Angela (1994), Symbiotic interactions, Oxford [Oxfordshire]: Oxford University Press, ISBN 0-19-854294-1Facey, Douglas E.; Helfman, Gene S.; Collette, Bruce B. (1997),The diversity of fishes, Oxford: Blackwell Science, ISBN 0-86542-256-7Golding, RS; Gupta, RS (1995), "Protein-based phylogenies support a chimeric origin for the eukaryotic genome", Mol. Biol. Evol. 12 (1): 1-6, PMID 7877484Harrison, Rhett (2002), "Balanced mutual use (symbiosis)",Quarterly journal Biohistory 10 (2), retrieved 2007-09-23Harrison, Maria J. (2005), "Signaling in the arbuscular mycorrhizal symbiosis", Annu. Rev. Microbiol. 59: 19-42,DOI:10.1146/annurev.micro.58.030603.123749,PMID 16153162Lee, J. (2003), "Amphiprion percula" (On-line), Animal Diversity Web, retrieved 2007-09-29Isaac, Susan (1992), Fungal-plant interactions, London: Chapman & Hall, ISBN 0-412-36470-0Isaak, Mark (2004), CB630: Evolution of obligate mutualism,TalkOrigins Archive, retrieved 2007-09-25Moran, N.A. (2006), "Symbiosis", Current Biology 16 (20): 866-871, DOI:10.1016/j.cub.2006.09.019, PMID 17055966, retrieved 2007-09-23Nardon, P.; Charles, H. (2002), "Morphological aspects of symbiosis", Symbiosis: Mechanisms and Systems. Dordercht/boson/London, Kluwer Academic Publishers4: 15-44, DOI:10.1007/0-306-48173-1_2Powell, Jerry (1992), "Interrelationships of yuccas and yucca moths", Trends in Ecology and Evolution 7 (1): 10-15,DOI:10.1016/0169-5347(92)90191-D, PMID 21235936Nair, S. (2005), "Bacterial Associations: Antagonism to Symbiosis", in Ramaiah, N, Marine Microbiology: Facets & Opportunities;, National Institute of Oceanography, Goa, pp. 83-89, retrieved 2007-10-12Roughgarden, J.; Gomulkiewicz; Holt; Thompson (1975), "Evolution of Marine Symbiosis--A Simple Cost-Benefit Model",Ecology 56 (5): 1201-1208, DOI:10.1046/j.1420-9101.2000.00157.x, JSTOR 1936160Saffo, M.B. (1993), "Coming to terms with a field: Words and concepts in symbiosis", Symbiosis. 14 (1-3), retrieved 2007-10-05Sagan, Dorion; Margulis, Lynn (1986), Origins of sex: three billion years of genetic recombination, New Haven, Conn: Yale University Press, ISBN 0-300-03340-0Sagan, Dorion; Margulis, Lynn (1997), Microcosmos: Four Billion Years of Evolution from Our Microbial Ancestors, Berkeley: University of California Press, ISBN 0-520-21064-6Sapp, Jan (1994), Evolution by association: a history of symbiosis, Oxford [Oxfordshire]: Oxford University Press,ISBN 0-19-508821-2Sapp, Jan (2009), The New Foundations of Evolution. On the Tree of Life, New York: Oxford University PressToller, W. W.; Rowan, R.; Knowlton, N. (2001), "Repopulation of Zooxanthellae in the Caribbean Corals Montastraea annularisand M. faveolata following Experimental and Disease-Associated Bleaching", The Biological Bulletin (Marine Biological Laboratory) 201(3): 360-373,DOI:10.2307/1543614, JSTOR 1543614,PMID 11751248Townsend, Colin R; Begon, Michael; Harper, John D. (1996),Ecology: individuals, populations and communities, Oxford: Blackwell Science, ISBN 0-632-03801-2Weiblen, G.D. (2002), "How to be a fig wasp", Annual Review of Entomology 47 (1): 299-330,DOI:10.1146/annurev.ento.47.091201.145213,PMID 11729077Wernegreen, J.J. (2004), "Endosymbiosis: lessons in conflict resolution", PLoS Biology 2 (3): e68,DOI:10.1371/journal.pbio.0020068, PMC 368163,PMID 15024418[edit]External linksTED-Education video - Symbiosis: a surprising tale of species cooperation.Wikimedia Commons has media related to: Symbiosis Look up symbiosis in Wiktionary, the free dictionary. [hide] vteInter-species biological interactions in ecologyAmensalismCommensalismInquilinismMutualismNeutralismSynnecrosisPredationCarnivoryHerbivoryIntraguildParasitismParasitoidismCheatingSymbiosisCleaning symbiosisCompetitionMimicryCategories:SymbiosisCreate accountLog inArticleTalkReadEditView historyMain pageContentsFeatured contentCurrent eventsRandom articleDonate to WikipediaInteractionHelpAbout WikipediaCommunity portalRecent changesContact WikipediaToolboxPrint/exportLanguagesAfrikaansالعربيةБеларуская‪беларуская (тарашкевіца)‬БългарскиCatalàČeskyDanskDeutschEestiΕλληνικάEspañolEsperantoEuskaraفارسیFrançaisGalego한국어हिन्दीHrvatskiIdoBahasa IndonesiaÍslenskaItalianoעבריתBasa Jawaಕನ್ನಡქართულიҚазақшаKreyòl ayisyenLatinaLatvie&scaron;uLietuviųMagyarМакедонскиမြန်မာဘာသာNederlands日本語‪norsk (bokmål)‬‪norsk (nynorsk)‬OromooPolskiPortuguêsRomânăРусскийSimple EnglishSlovenčinaSloven&scaron;činaСрпски / srpskiSuomiSvenskaTagalogதமிழ்Татарча/tatarçaУкраїнська中文This page was last modified on 15 July 2012 at 01:44.Text is available under the Creative Commons Attribution-ShareAlike License; additional terms may apply. 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